Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study evaluated the dose-related trophic effects of glutamine, gastrin, and somatostatin on the in vitro growth of human gastric cancer cells and normal human gastric mucosal cells. Quadruplicate cell cultures were seeded into growth medium with or without glutamine, gastrin, or somatostatin. After 72 hours' incubation, cells were counted and their numbers compared with those of controls. Glutamine and gastrin stimulated the growth of both normal and malignant gastric mucosal cells. Compared with normal cells, the malignant cells responded to these growth factors at lower concentrations. Somatostatin enhanced growth of gastric cancer cells at all concentrations and inhibited growth of normal cells at high concentrations. Further studies on the responsiveness of gastric adenocarcinoma to gastrointestinal tract hormones may elucidate mechanisms of oncogenesis and suggest new therapeutic avenues for patients with gastric cancer.
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PMID:Effects of gastrin, glutamine, and somatostatin on the in vitro growth of normal and malignant human gastric mucosal cells. 286 4

The presence of somatostatin (SRIF) in the neoplastic epithelial cells of certain Warthin's tumors arising in the human parotid gland was found immunohistochemically, whereas the other parotid gland tumors, such as pleomorphic adenoma, oxyphilic adenoma, mucoepidermoid tumor, adenocarcinoma, and adenoid cystic carcinoma, did not show positive immunoreactivity for SRIF. The SRIF-positive Warthin's tumor had dense core granules immunoreactive with anti-SRIF serum. Moreover, a comparatively high concentration of immunoreactive SRIF was detected by radioimmunoassay in an SRIF-positive Warthin's tumor, although the other tumors also contained low levels of immunoreactive SRIF.
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PMID:Immunoreactive somatostatin in Warthin's tumor. 287 59

Pancreatic ductal adenocarcinoma was induced in female Syrian golden hamsters by injecting N-nitrosobis(2-oxopropyl)amine (BOP) once a week at a dose of 10 mg per kg of body weight for 18 weeks. Hamsters were then treated with somatostatin analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) or with [6-D-tryptophan]luteinizing hormone-releasing hormone [( D-Trp6]LH-RH) delayed delivery systems. Microcapsules of somatostatin analog RC-160, designed to release a dose of 5 micrograms/day, were injected twice a month and microcapsules of [D-Trp6]LH-RH, calculated to liberate 25 micrograms per day, once a month. After 18 weeks of BOP administration, the hamsters were divided into three groups of 10-20 animals each. Group I consisted of untreated controls, group II was injected with RC-160, and group III was injected with [D-Trp6]LH-RH. A striking decrease in tumor weight and volume was obtained in animals treated with [D-Trp6]LH-RH or with the somatostatin analog RC-160. After 45 days of treatment with either analog, the survival rate was significantly higher in groups II and III (70%), as compared with the control group (35%). The studies, done by light microscopy, high-resolution microscopy, and electron microscopy, showed a decrease in the total number of cancer cells and changes in the epithelium, connective tissue, and cellular organelles in groups II and III treated with the hypothalamic analogs as compared to controls. These results in female hamsters with induced ductal pancreatic tumors confirm and extend our findings, obtained in male animals with transplanted tumors, that [D-Trp6]LH-RH and somatostatin analogs inhibit the growth of pancreatic cancers.
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PMID:Treatment of nitrosamine-induced pancreatic tumors in hamsters with analogs of somatostatin and luteinizing hormone-releasing hormone. 288 Dec 96

This study was undertaken to assess the prevalence and characteristic hormonal profile of endocrine cells in Barrett's mucosa and to determine to what extent this profile was shared by endocrine cells of adenocarcinomas arising therefrom. In addition, lower oesophageal carcinomas, not associated with columnar metaplasia, were examined to see if they exhibited a different hormonal profile. The patients studied comprised 43 who had had multiple oesophageal biopsies. 35 who had had oesophagogastric resection for adenocarcinoma arising in Barrett's mucosa and 26 in whom the resection showed no metaplastic epithelium adjacent to tumour. Argyrophil cells were present in 90% of biopsies and resections of Barrett's mucosa combined, irrespective of the histological type of metaplastic epithelium. By immunocytochemistry the most frequently identified substance in mucosal endocrine cells was serotonin (82%) followed by somatostatin (54%), secretin (22%) and pancreatic polypeptide (17%). Gastrin, bombesin, cholecystokinin, ACTH and substance P were not identified in metaplastic mucosa in any case. The difference in expression of serotonin by endocrine cells of tumours arising in Barrett's mucosa (31%) and those not (3.8%) was statistically significant (P less than 0.0186). Carcinoembryonic antigen (CEA) was demonstrated in 60% of oesophageal carcinomas, both endocrine positive and endocrine negative. Focal CEA expression was seen in 4.6% of biopsies and 14% of Barrett's mucosa adjacent to tumour. These results indicate a higher prevalence of endocrine cells in Barrett's mucosa than hitherto documented and suggest that serotonin may be a useful marker in distinguishing between primary oesophageal and putative gastric cancers at the gastro-oesophageal junction. The identification of CEA in oesophageal columnar epithelium is of little value in predicting the development of malignancy.
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PMID:The relationship of endocrine cells, dysplasia and carcinoembryonic antigen in Barrett's mucosa to adenocarcinoma of the oesophagus. 288 73

A case of prostatic carcinoma with the cellular patterns of an adenocarcinoma and carcinoid tumor is reported. The tumor contained ultrastructural dense core neuroendocrine granules, and immunoperoxidase staining revealed prostatic acid phosphatase, prostatic-specific antigen, chromogranin, neuron-specific enolase, serotonin, adrenocorticotrophic hormone (ACTH), somatostatin, parathormone, calcitonin, bombesin, and glucagon but no insulin. The patient had exhibited hypercalcemia that may have been related to hormone production by the tumor. The literature on the endocrine aspect of the prostate and its tumor is reviewed.
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PMID:Prostatic carcinoma with endocrine features. A report of a neoplasm containing multiple immunoreactive hormonal substances. 289 Dec 93

Membrane receptors for luteinizing hormone-releasing hormone (LH-RH), somatostatin, and prolactin (PRL) were investigated in the Dunning R-3327H rat prostate adenocarcinoma specimens after in vivo treatment with microcapsules of the agonist [D-Trp6]LH-RH and the somatostatin analog RC-160. The LH-RH receptors showed a low-binding affinity (Kd = 54 nM) and high capacity (Bmax = 12.0 pmol/mg). Treatment with the [D-Trp6]LH-RH decreased the binding affinity (Kd = 0.52 microM). Specific somatostatin receptors, with Kd = 1.3 nM and Bmax = 543 fmol/mg, were also found. Treatment with [D-Trp6]LH-RH lowered Bmax to 44 fmol/mg, and administration of RC-160 reduced Kd to 30 nM. After the combined treatment with the two analogs, Kd and Bmax were decreased. Specific PRL receptors (Kd = 0.72 nM; Bmax = 161 fmol/mg) were also detected. Treatment with either analog reduced Bmax by 50%, but a much greater reduction of PRL binding capacity was revealed after in vitro dissociation of the bound endogenous PRL by MgCl2. The dramatic fall in the total number of PRL receptors after combination treatment with both analogs could be partially responsible for the decrease in the weight and volume of prostate tumors. The findings support the concept that analogs of LH-RH and somatostatin can inhibit tumors directly through their own respective receptors. One of several mechanisms of the antineoplastic activity of these analogs could be the elimination of tumor growth-promoting effect of PRL by the reduction of the total number of PRL receptors.
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PMID:Receptors for prolactin, somatostatin, and luteinizing hormone-releasing hormone in experimental prostate cancer after treatment with analogs of luteinizing hormone-releasing hormone and somatostatin. 289 78

Somatostatin receptor frequency was evaluated in 12 human exocrine pancreatic carcinomas taken after surgery. The tumors were analyzed by receptor autoradiography on tissue sections and by in vitro binding techniques on tumor homogenates. None of the tested human pancreatic carcinomas was shown to possess specific somatostatin receptors. In comparison, five single tumors taken from rats transplanted with the rat pancreatic adenocarcinoma CA 20948 were found to contain specific high-affinity somatostatin receptors. Also, human endocrine pancreatic tumors, i.e., two insulinomas, did contain somatostatin receptors under identical experimental conditions. These data confirm previous results with other tumors, documenting the absence of somatostatin receptors in highly malignant human carcinomas. They also may represent an explantation at the molecular level for the lack of therapeutic effect of somatostatin analogues such as SMS 201-995 seen in patients with advanced exocrine pancreatic carcinomas.
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PMID:Absence of somatostatin receptors in human exocrine pancreatic adenocarcinomas. 289 30

The effects of gastrin, proglumide (a gastrin receptor antagonist), and somatostatin on growth of human colon adenocarcinoma cell lines CX1, X56, and HT29 were examined in two experimental models. Nude mice bearing xenografts of colon cancer CX1 or X56 were treated for 14-25 days subcutaneously with saline, pentagastrin (0.5 or 1.0 mg/kg), proglumide (250 or 500 mg/kg), or somatostatin 14 (33, 100, or 300 micrograms/kg) twice daily. Tumor volume, weight, protein, and deoxyribonucleic acid were measured. HT29 cells were grown in vitro and the effects of gastrin 17, proglumide, and somatostatin on growth were evaluated by cell counts or [3H]thymidine incorporation. The larger dose of pentagastrin significantly increased tumor growth in the nude mouse (p less than 0.005) and gastrin induced a biphasic effect on deoxyribonucleic acid synthesis in tissue culture with significant increases of up to 39% (p less than 0.025). Somatostatin alone significantly inhibited tumor growth in two of the cell lines and also inhibited the gastrin-induced growth. Proglumide had no effect by itself but significantly inhibited gastrin-stimulated growth. These findings suggest that growth of some human colon cancers may be hormone-dependent.
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PMID:Effects of gastrin, proglumide, and somatostatin on growth of human colon cancer. 290 11

The prevalence of endocrine differentiation of conventional gastric adenocarcinoma was evaluated on the 212 cases (including 62 mucosal carcinomas) of consecutively resected stomach for adenocarcinoma in our hospital using anti-chromogranin A (CGA) antibodies. CGA-positive cells were found in 28 of 150 cases (18.7%) as an integral tumor component. In immunocytochemistry and electron microscopic examinations, we could classify these 28 cases into three groups according to the distribution patterns of CGA-positive cells. The first group consisted of 12 cases in which scattered CGA-positive cells were located in neoplastic glands. The second group consisted of six cases of scirrhous carcinoma in which CGA-positive cells were separated by fibrovascular tissue. The third group consisted of ten cases in which the positive cells were present in clusters. No definite correlation was recognized between the appearance of CGA cells and histologic types of predominance. In the analysis of the hormonal substances coexpressed by CGA-positive cells, immunoreactive serotonin (SER) was found most frequently, and somatostatin (SS), gastrin (GAS), glucagon/glicentin (GLU/GLI), and peptide-tyrosine-tyrosine (PYY) like immunoreactivities were found in a few tumor cells. CGA-positive cells occupied limited parts of the tumors in most cases, and they were noticeably more frequent in advanced stage cases. This might explain why endocrine differentiation reflects the dysexpression of the neoplastic stem cells. Furthermore, absence of mitotic figures in this type of cell and negativity of a single colony composed exclusively of CGA cells in metastatic foci suggested that these cells are in a dormant phase and are probably postmitotic.
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PMID:Endocrine differentiation of gastric adenocarcinoma. The prevalence as evaluated by immunoreactive chromogranin A and its biologic significance. 304 73

An endocrine cell carcinoma of the extrahepatic bile duct in a 79-year-old man is described. The patient had complaints of jaundice and epigastric pain due to a small tumor located at the confluence of the common hepatic duct with the cystic duct. Microscopically, the tumor showed a well differentiated tubular adenocarcinoma and was confined to the mucosa. Numerous tumor cells showed argyrophil and/or argentaffin reactions. Immunoperoxidase staining revealed that the tumor tissue contained somatostatin-, gastrin-and serotonin-immunoreactive cells. From these findings the tumor was diagnosed as endocrine cell carcinoma. Four years later he remains well without any evidence of recurrence or metastasis. The histogenesis of endocrine cells in the biliary tract is briefly discussed.
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PMID:Endocrine cell carcinoma of extrahepatic bile duct. 352 8


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